L-Glutamate, a major neurotransmitter in the central nervous system, has been known to be extensively released during brain ischemia and induces subsequent neuronal cell death1'2). Recent studies indicate that oxygen radicals are produced through a variety of intracellular cascades in such events2). It was also reported that blockage of glutamate toxicity by free radical scavengers was effective to ameliorate brain ischemia injury3'4). Recently, some glutamate toxicity inhibitors of microbial origin such as carquinostatin A5), lavanduquinocin6), and aestivophoenins A and B7) have been reported. In the course of our screening for free radical scavengers or inhibitors of glutamate toxicity using the neuronal hybridoma N18-RE-105 cells to prevent the brain ischemia injury, we previously isolated benzastatins A~G8~10) and phenazostatins A~Cn~13). Further investigation on polar metabolites of Streptomyces nitrosporeus 30643 which is the producer of benzastatins A-G has resulted in isolation of two hydroxylated derivatives of benzastatin B (3), benzastatins H (1) and I (2) (Fig. 1). We report here the isolation, physico-chemical properties, structure determination, and biological activities of 1 and 2.